All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
Fuad N Ziyade. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. Journal of the American Society of Nephrology : JASN. vol 15 Suppl 1. 2004-05-25. PMID:14684674. treatment of diabetic mice with neutralizing anti-tgf-beta antibodies prevents the development of renal hypertrophy, mesangial matrix expansion, and the decline in renal function. 2004-05-25 2023-08-12 mouse
Fuad N Ziyade. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. Journal of the American Society of Nephrology : JASN. vol 15 Suppl 1. 2004-05-25. PMID:14684674. these studies argue strongly in support of the hypothesis that overactivity of the tgf-beta system in the kidney is a crucial mediator of diabetic renal hypertrophy and mesangial matrix expansion. 2004-05-25 2023-08-12 mouse
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. it is hypothesized that changes in the genes of cytokines, extracellular matrix proteins, and proteins regulating programmed cell death are related to hypertrophic scar formation. 2004-05-20 2023-08-12 Not clear
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. no change in these matrix metalloproteinases could be shown with il-6 stimulation in hypertrophic scar fibroblasts. 2004-05-20 2023-08-12 Not clear
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. the absence of any up-regulation of mmp-1 and mmp-3 in hypertrophic scar fibroblasts, in response to il-6, suggests that suppression of matrix metalloproteinases may play a role in the excessive accumulation of collagen formed in hypertrophic scars. 2004-05-20 2023-08-12 Not clear
Cynthia M Coleman, Rocky S Tua. Growth/differentiation factor 5 enhances chondrocyte maturation. Developmental dynamics : an official publication of the American Association of Anatomists. vol 228. issue 2. 2004-05-19. PMID:14517992. exposure to gdf5 significantly enhanced chondrocyte hypertrophy and maturation, as determined by the presence of alkaline phosphatase activity, collagen type x protein production, and the presence of a sulfated proteoglycan-rich extracellular matrix. 2004-05-19 2023-08-12 chicken
Guoyan Wang, Anita Woods, Shalev Sabari, Luca Pagnotta, Lee-Anne Stanton, Frank Beie. RhoA/ROCK signaling suppresses hypertrophic chondrocyte differentiation. The Journal of biological chemistry. vol 279. issue 13. 2004-05-07. PMID:14726536. rhoa overexpression in chondrogenic atdc5 cells results in increased proliferation and a marked delay of hypertrophic differentiation, as shown by decreased induction of alkaline phosphatase activity, mineralization, and expression of the hypertrophic markers collagen x, bone sialoprotein, and matrix metalloproteinase 13. 2004-05-07 2023-08-12 Not clear
Cornelia Piper, Heinz-Peter Schultheiss, Daniel Akdemir, Joern Rudolf, Dieter Horstkotte, Matthias Pauschinge. Remodeling of the cardiac extracellular matrix differs between volume- and pressure-overloaded ventricles and is specific for each heart valve lesion. The Journal of heart valve disease. vol 12. issue 5. 2004-04-27. PMID:14565712. different patterns of fibroblast-mediated remodeling of the extracellular matrix (ecm) might be expected between patients with pressure- and volume-induced left ventricular hypertrophy. 2004-04-27 2023-08-12 Not clear
Lee-Anne Stanton, Shalev Sabari, Arthur V Sampaio, T Michael Underhill, Frank Beie. p38 MAP kinase signalling is required for hypertrophic chondrocyte differentiation. The Biochemical journal. vol 378. issue Pt 1. 2004-04-22. PMID:14594450. in addition, p38 inhibition causes reduced expression of hypertrophic marker genes such as collagen x, matrix metalloproteinase 13 and bone sialoprotein. 2004-04-22 2023-08-12 mouse
Rethinasamy Prabhakar, Natalia Petrashevskaya, Arnold Schwartz, Bruce Aronow, Greg P Boivin, Jeffery D Molkentin, David F Wieczore. A mouse model of familial hypertrophic cardiomyopathy caused by a alpha-tropomyosin mutation. Molecular and cellular biochemistry. vol 251. issue 1-2. 2004-04-16. PMID:14575301. a dna hybridization microarray analysis of the transgenic vs. control ventricular rnas shows that 50 transcripts are differentially expressed by more than 100% during the onset of the hypertrophic process, many of which are associated with the extracellular matrix. 2004-04-16 2023-08-12 mouse
Mohammed Shakil Ahmed, Erik Øie, Leif Erik Vinge, Arne Yndestad, Geir Øystein Andersen G, Yvonne Andersson, Toril Attramadal, Håvard Attramada. Induction of myocardial biglycan in heart failure in rats--an extracellular matrix component targeted by AT(1) receptor antagonism. Cardiovascular research. vol 60. issue 3. 2004-04-16. PMID:14659801. cardiac remodelling associated with congestive heart failure typically involves dilatation of the ventricular cavities, cardiomyocyte hypertrophy and alterations of extracellular matrix. 2004-04-16 2023-08-12 rat
Kwong Man Lee, Alfred Sze Lok Cheng, Wing Hoi Cheung, Pauline Po Yee Lui, Vincent Ooi, Kwok Pui Fung, Ping Chung Leung, Kwok Sui Leun. Bioengineering and characterization of physeal transplant with physeal reconstruction potential. Tissue engineering. vol 9. issue 4. 2004-04-07. PMID:13678448. they synthesized and deposited cartilaginous matrix and differentiated into hypertrophic chondrocytes marked by increases in cell size and alkaline phosphatase activity. 2004-04-07 2023-08-12 Not clear
Dengshun Miao, Hanlong Liu, Paul Plut, Meijuan Niu, Rujuan Huo, David Goltzman, Janet E Henderso. Impaired endochondral bone development and osteopenia in Gli2-deficient mice. Experimental cell research. vol 294. issue 1. 2004-03-30. PMID:14980515. the growth plates of tibiae and vertebrae exhibited increased numbers of proliferating and hypertrophic chondrocytes with no apparent alteration in matrix mineralisation. 2004-03-30 2023-08-12 mouse
Shunichi Shibata, Naoto Suda, Kenji Fukada, Kimie Ohyama, Yasuo Yamashita, Vicki E Hammon. Mandibular coronoid process in parathyroid hormone-related protein-deficient mice shows ectopic cartilage formation accompanied by abnormal bone modeling. Anatomy and embryology. vol 207. issue 1. 2004-03-24. PMID:12768421. in situ hybridization of matrix proteins showed that this coronoid cartilage had characteristics of the lower hypertrophic cell zone usually present at the site of endochondral bone formation and/or "chondroid bone" occasionally found in distraction osteogenesis. 2004-03-24 2023-08-12 mouse
Sheldon Chen, Belinda Jim, Fuad N Ziyade. Diabetic nephropathy and transforming growth factor-beta: transforming our view of glomerulosclerosis and fibrosis build-up. Seminars in nephrology. vol 23. issue 6. 2004-03-24. PMID:14631561. prominent among these is transforming growth factor beta (tgf-beta) because it promotes renal cell hypertrophy and stimulates extracellular matrix accumulation, the 2 hallmarks of diabetic renal disease. 2004-03-24 2023-08-12 human
Sheldon Chen, Belinda Jim, Fuad N Ziyade. Diabetic nephropathy and transforming growth factor-beta: transforming our view of glomerulosclerosis and fibrosis build-up. Seminars in nephrology. vol 23. issue 6. 2004-03-24. PMID:14631561. in tissue culture studies, cellular hypertrophy and matrix production are stimulated by high glucose concentrations in the culture media. 2004-03-24 2023-08-12 human
M I Pavlov, J-M Sautier, M Oboeuf, A Asselin, A Berda. Chondrogenic differentiation during midfacial development in the mouse: in vivo and in vitro studies. Biology of the cell. vol 95. issue 2. 2004-03-17. PMID:12799063. the purpose of this second part was to assess if chondrocytes could further differentiate in vitro until the hypertrophic phase and matrix mineralization. 2004-03-17 2023-08-12 mouse
Yoshiko Sawae, Takako Sahara, Takahisa Sasak. Osteoclast differentiation at growth plate cartilage-trabecular bone junction in newborn rat femur. Journal of electron microscopy. vol 52. issue 6. 2004-03-12. PMID:14756237. in the growth plate cartilage, thin mineralized areas were detected solely in the longitudinal septal cartilage matrix in the hypertrophic zone, but the transverse septal cartilage matrix between adjacent chondrocytic lacunae within a row of chondrocytes remained unmineralized. 2004-03-12 2023-08-12 rat
Michelle R Campbell, Catherine J Gress, Elizabeth H Appleman, Olena Jacenk. Chicken collagen X regulatory sequences restrict transgene expression to hypertrophic cartilage in mice. The American journal of pathology. vol 164. issue 2. 2004-03-11. PMID:14742255. nature 1993, 365:56-61; jacenko o, chan d, franklin a, ito s, underhill cb, bateman jf, campbell mr: a dominant interference collagen x mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice. 2004-03-11 2023-08-12 mouse
Haruhito Azuma, Teruo Inamoto, Takeshi Sakamoto, Satoshi Kiyama, Takanobu Ubai, Yuko Shinohara, Kentaro Maemura, Motomu Tsuji, Naoki Segawa, Hiroshi Masuda, Kiyoshi Takahara, Yoji Katsuoka, Masahito Watanab. Gamma-aminobutyric acid as a promoting factor of cancer metastasis; induction of matrix metalloproteinase production is potentially its underlying mechanism. Cancer research. vol 63. issue 23. 2004-02-27. PMID:14678958. we investigated expression of gamma-aminobutyric acid (gaba), glutamate decarboxylase, and matrix metalloproteinase (mmp) in the prostates of patients with cancer or benign prostatic hypertrophy by immunohistochemical study. 2004-02-27 2023-08-12 human